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Objective To investigate the predictive value of heart rate-corrected QT (QTc) and heart rate-corrected Tp-Te (Tp-Tec) intervals combined with serum complement 1q/tumor necrosis factor-related protein 9 (CTRP9) levels for the development of ventricular arrhythmias (VA) after acute myocardial infarction (AMI). Methods A total of 156 patients with AMI were selected, VA occurred in 61 cases during hospitalization (VA group), and 95 cases (non-VA group) did not have VA. The QT and Tp-Te intervals were recorded on admission using a 12-lead ECG machine, and the QTc and Tp-Tec intervals were calculated. On the next day of admission, early morning fasting elbow venous blood was collected, centrifuged and serum was retained, and serum CTRP9 was measured by ELISA. We compared the general clinical data［including gender, age, BMI, smoking history, underlying diseases (hypertension, diabetes, hyperlipidemia)], disease-related data［including Killip classification on admission, left ventricular ejection fraction (LVEF) within 6 h after admission], laboratory examination data [including the four lipid items (TC, TG, HDL-C, LDL-C), blood creatinine (Scr), blood uric acid (UA), fasting plasma glucose (FPG) and serum CTRP9 level on the day after admission] and ECG examination data (including QTc, Tp-Tec interval) between the two groups. A multi-factor Logistic regression model was used to analyze the factors influencing the development of VA after AMI. Receiver operating characteristic (ROC) curves were used to analyze the predictive value of QTc, Tp-Tec intervals and serum CTRP9 levels in the development of VA after AMI. Results Compared with the non-VA group, the QTc and Tp-Tec intervals were significantly prolonged and serum CTRP9 levels were significantly lower in the VA group (all P<0. 05). No significant differences were found in the general clinical data and blood lipid, FPG, or Scr between the two groups (all P>0. 05). The ratio of Killip grade >Ⅱ in the VA group was higher than that in the non-VA group, while the LVEF was lower than that in the non-VA group (both P<0. 05). UA was higher in the VA group than in the non-VA group (P<0. 05). Multi-factor Logistic regression analysis showed that UA, QTc interval and Tp-Tec interval were all independent risk factors for the development of VA after AMI, while CTRP9 was an independent protective factor (all P<0. 05). ROC curve analysis showed that the area under the curve (AUC) for QTc and Tp-Tec intervals combined with serum CTRP9 levels in predicting VA after AMI was significantly higher than that of QTc interval, Tp-Tec interval, QTc interval + Tp-Tec interval, and CTRP9 in predicting VA after AMI (all P<0. 01). Conclusions Patients with VA after AMI had significantly longer QTc and Tp-Tec intervals and significantly lower serum CTRP9 levels. QTc and Tp-Tec intervals were independent risk factors for the development of VA after AMI, while CTRP9 was its independent protective factor. QTc, Tp-Tec intervals and serum CTRP9 levels all had some predictive value for the development of VA after AMI, but QTc and Tp-Tec intervals combined with serum CTRP9 levels had significantly higher predictive value for the development of VA after AMI. [ABSTRACT FROM AUTHOR]

Objective To identify the chemical components of Guanxin H formula, and explore its mechanism in the treatment of acute myocardial infarction. Methods In this study, the components of Guanxin H formula were identified w让h high performance liquid chromatography-mass spectrometrytandem mass spectrometry (HPLC-MS/MS), the targets of the detected components were screened by searching the TCMSP database, and the disease targets were screened by searching the GeneCards and OMIM databases. Then STRING was applied to build the network of PPI, and Bioconductor database was used to perform GO and KEGG enrichment analysis, and Cytoscape software was used to build the drug・ component-target-pathway-disease network diagram・ Core targets were then obtained by calculating topological parameters・ Finally, detected components and targets were identified by molecular docking・ Results Five chemical components of Guanxin H formula were detected, i・ e. ferulic acid, tanshinol, paeoniflorin, protocatechualdehyde, and hydroxysafflor yellow A (HSYA)・ Nine key targets were screened, including CHRM1, CHRM2, CHRM3, PTGS1, ADRA1A, PLAU, GABRA1, AR and IL6, with the neuroactive ligand-receptor interaction pathway, calcium signaling pathway, cholinergic synapse pathway, and actin cytoskeleton signaling pathway involved・ Molecular docking showed good binding activity between the detected components and CHRM1, and the molecular conformation was stable・ Conclusion Five quality control components of Guanxin H formula could be detected relatively quickly and accurately by HPLC-MS/MS・ By binding with CHRM1, the components of Guanxin H seem to protect cardiac myocytes through regulating the neuroactive ligand-receptor interaction pathway, calcium signaling pathway, cholinergic synapse pathway, and actin cytoskeleton signaling pathway, thus inhibiting oxidative stress, inflammatory damage and apoptosis after myocardial infarction. This study potentially provides a new idea and direction for further exploring the mechanism of Guanxin H formula in the treatment of acute myocardial infarction. However, further experimental proof is still needed to determine whether Guanxin H formula plays a role through the four pathways above, and to clarify the main targets and interaction between pathways. [ABSTRACT FROM AUTHOR]